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Published in Henry J. Woodford, Essential Geriatrics, 2022
Epilepsy has a bimodal peak of incidence, with a first spike in childhood and a second larger peak over age 75. The prevalence is around 0.8% in people aged over 85 and may be as high as 7.5% among nursing home residents.38,39 Epilepsy can be idiopathic or secondary to underlying structural brain changes. In older people, idiopathic epilepsy is rare. Seizures secondary to cerebrovascular disease account for 30–40% of cases.40 Seizures occur in 10–20% of people with advanced dementia, and this represents 10–20% of epilepsies in older adults.40,41 Tumours, subdural haematomas, drugs (e.g. antidepressants, antipsychotics, theophylline, baclofen or benzodiazepine withdrawal), alcohol or metabolic disturbances (e.g. hypoglycaemia or hyponatraemia) can also provoke seizures. Seizures can be focal (localised symptoms) or generalised (affecting most of the brain). Examples of generalised seizures include tonic-clonic episodes and absences. Focal seizures can affect consciousness (then termed ‘focal dyscognitive seizures'). Focal seizures can also become secondarily generalised, e.g. localised symptoms followed by a tonic-clonic seizure. In older adults around 70% of seizures are of focal onset, with or without secondary generalisation.42 Non-convulsive status epilepticus is discussed on page 156. Transient epileptic amnesia is discussed on page 229.
Epilepsy
Published in Philip B. Gorelick, Fernando D. Testai, Graeme J. Hankey, Joanna M. Wardlaw, Hankey's Clinical Neurology, 2020
Donald C. Barr, Andres M. Kanner
The second implication relates to the difficulty of diagnosing seizures in patients with AD, as the majority of seizures in patients with dementia are nonconvulsive.35,36 Sudden episodes of worsened cognition postictally can be interpreted as an ordinary fluctuation of the AD condition. Besides, as the patient has memory impairment, it can prove difficult for him or her to remember an unusual episode, especially in the case of a nonconvulsive seizure.37 This is particularly evident in conditions such as transient epileptic amnesia (TEA), a condition consisting of rather short (usually <1 hour) episodes of amnesia, and their repetitive occurrence should prompt clinicians to distinguish this treatable form of temporal lobe epilepsy (TLE) from transient global amnesia, which has epileptiform abnormalities on EEG, and a clear-cut response to AEDs.37,38
Dementia
Published in John W. Scadding, Nicholas A. Losseff, Clinical Neurology, 2011
Seizures themselves may cause cognitive deficits. Transient epileptic amnesia is recognized as a cause of cognitive impairment, producing discrete episodes of amnesia for events. It primarily affects middle-aged people. Episodes are brief and recurrent, often on waking. EEG may show temporal lobe spikes; MRI may show evidence of hippocampal damage. The episodes respond to antiepileptic drugs, but there may be residual interictal deficits.
The overlap between epilepsy and Alzheimer’s disease and the consequences for treatment
Published in Expert Review of Neurotherapeutics, 2019
Graham Powell, Besa Ziso, AJ Larner
It was initially thought that generalized seizures, presumably secondarily generalized from a partial seizure focus, predominated in AD [16], and that complex partial seizures may also occur but might be under-recognized in the context of progressive dementia [26]. These conclusions may simply have been a reflection of ascertainment bias. More subtle changes may easily be overlooked. Occasional cases of transient epileptic amnesia (TEA) have been described in the early stages of AD [27,28] and suggested as a contributory factor to wandering behavior exhibited by some AD patients [29]. At the other end of the epilepsy spectrum, status epilepticus, of complex partial [30] or non-convulsive [31] type, has been described on occasion in association with AD. A recent study using a proforma to elicit symptoms suggestive of epilepsy in patients with AD and mild cognitive impairment (MCI) identified a broad range of seizure-related phenomena, including altered responsiveness, automatisms (oral, pharyngeal), auras (olfactory, gustatory), arrest of speech or behaviour, focal motor seizures, sensory phenomena including hallucinations, and amnesia on waking (typical of TEA). Most seizures were subtle and non-convulsive and hence easily missed [32].